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Cellular Senescence in Age-Related Macular Degeneration: Can Autophagy and DNA Damage Response Play a Role?

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Date
2017
Author(s)
Blasiak Janusz
Piechota Malgorzata
Pawlowska Elzbieta
Szatkowska Magdalena
Sikora Ewa
Kaarniranta Kai
Unique identifier
10.1155/2017/5293258
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Citation
Blasiak Janusz. Piechota Malgorzata. Pawlowska Elzbieta. Szatkowska Magdalena. Sikora Ewa. Kaarniranta Kai. (2017). Cellular Senescence in Age-Related Macular Degeneration: Can Autophagy and DNA Damage Response Play a Role?.  Oxidative Medicine and Cellular Longevity, 2017, 5293258. 10.1155/2017/5293258.
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CC BY http://creativecommons.org/licenses/by/4.0/
Abstract

Age-related macular degeneration (AMD) is the main reason of blindness in developed countries. Aging is the main AMD risk factor. Oxidative stress, inflammation and some genetic factors play a role in AMD pathogenesis. AMD is associated with the degradation of retinal pigment epithelium (RPE) cells, photoreceptors, and choriocapillaris. Lost RPE cells in the central retina can be replaced by their peripheral counterparts. However, if they are senescent, degenerated regions in the macula cannot be regenerated. Oxidative stress, a main factor of AMD pathogenesis, can induce DNA damage response (DDR), autophagy, and cell senescence. Moreover, cell senescence is involved in the pathogenesis of many age-related diseases. Cell senescence is the state of permanent cellular division arrest and concerns only mitotic cells. RPE cells, although quiescent in the retina, can proliferate in vitro. They can also undergo oxidative stress-induced senescence. Therefore, cellular senescence can be considered as an important molecular pathway of AMD pathology, resulting in an inability of the macula to regenerate after degeneration of RPE cells caused by a factor inducing DDR and autophagy. It is too early to speculate about the role of the mutual interplay between cell senescence, autophagy, and DDR, but this subject is worth further studies.

URI
https://erepo.uef.fi/handle/123456789/5753
Link to the original item
http://dx.doi.org/10.1155/2017/5293258
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Hindawi Limited
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  • Terveystieteiden tiedekunta [1335]
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